ECG Teaser


Here are the “can’t miss” ECG’s that you need to be able to recognise for the exam. In the VAQ section you only have 7.5 minutes to write your answers, and in the SCE you may only have a minute or two to discuss the ECG, so if you can “spot diagnose” some of these notoriously difficult ECGs’, you will save time, and allow yourself more time time to write/decribe your answer. Also stating the diagnosis early demonstrates a higher level of knowledge than someone who has to figure it out step by step (but READ or LISTEN to the QUESTION CLOSELY – and answer it as per the GLOSSARY DEFINED TERMS).


ECG’s are a topic that as per the syllabus require expert level knowledge, so try your skills on these:


ECG 1:

A 25 year old man presents with palpitations and dizziness.  His BP is 80/40. Decribe and interpret his ECG (click to enlarge).

wpw af1

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Wolf Parkinson White and Atrial Fibrillation.

Why is this important? WPW involves conduction of impulses via an “accessory pathway” (the so called Bundle of Kent). This can occur in either an anterograde or retrograde fashion, depending on which way the impulse is travelling – either orthodromic or antidromic.  If the patient with WPW has a REGULAR narow complex tachycardia (or simple SVT) and you administer one of the usual AV-nodal blocking drugs, the SVT rate (usually 160-180bpm) will divert down the non-rate-limited Bundle of Kent and stimulate the ventricles at the same rate, which will give you a very fast heart rate, but is unlikley to kill you.  If however you misdiagnose THIS ECG (ie AF & WPW) as simple SVT and administer adenosine or verapamil, or diagnose it as simple AF and give metoprolol or digoxin, the atrial rate (which is around 300 in AF) will be transmitted down the accessory pathway (as you’ve blocked the AV node) and stimulate the ventricles at this rate. A ventricular rate of 300 = VF = bad news.  Therefore the “safest” treatment for this case is synchronised DC reversion.  There are pharamcological options, and there are varying opinions on which drug is best options include procainamide, flecainide, and believe it or not, amiodarone). We’ll do a bit of a search and see what the latest opinion is & let you know… Definitve treatment to prevent recurrence is catheter ablation by an Electrophysiologist.




A 34 year old man presents after a syncopal episode. Describe & Interpret his ECG:



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Hypertrophic (Obstructive) Cardiomyopathy.

This ECG shows sinus rhythm with several atrial premature beats/ectopics.  The striking feature is that of left ventricular hypertrophy, small inferior/lateral q-waves and deep infero-lateral T-wave inversion (the so called “strain” pattern).

Any time you see an ECG that meets LVH criteria in a young person with syncope, think “HOCM”!

Why is this important? This condition is associated with “SCD” or “sudden cardiac death”.  This is either from arrhythmias (VT/VF) or ischemia (due to the enlarged left ventricles increased oxygen sonsumption).  The risk of SCD is relatively “low” but is still siginficant, around 1% in adults, but much higher (6%) in children.

Click here for a nice, concise summary about HOCM.

Here is another simple description from Wikipedia.


The above ECG is a fairly obvious case, but beware that HOCM can present with more subtle ECG manifestations. The following ECG’s show some of the other findings such as septal hypertrophy (large R waves in v2-4) which may be mis-interpreted as “normal R-wave progression”, and q-waves (see arrows) which one would not expect to see in a young person with a structurally normal heart after a “fainting episode”.  Hopefully in practice you’d still recognise the grossly abnormal T-wave inversion and not discharge the patient home, but in the exam you’ll do better if you pick it as HOCM and admit the patient for monitoring and an Echo!


How confident are you at diagnosing LVH? It is usually quite obvious, but in the exam it may be useful to have some criteria that you can espouse.  Don’t try and memorise all of them, but it’s worth knowing one set of criteria.

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There are several sets of criteria used to diagnose LVH via electrocardiography.  None of them is perfect, though by using multiple criteria sets, the sensitivity and specificity are increased.

The Sokolow-Lyon index    

  • S in V1 + R in V5 or V6 (whichever is larger) ≥ 35 mm (≥ 7 large squares)
  • R in aVL ≥ 11 mm

The Cornell voltage criteria for the ECG diagnosis of LVH involves measurement of the sum of the R wave in lead aVL and the S wave in lead V3. The Cornell criteria for LVH are:

  • S in V3 + R in aVL > 28 mm (men)
  • S in V3 + R in aVL > 20 mm (women)

Romhilt-Estes point score system (“diagnostic” >5 points; “probable” 4 points):

ECG Criteria Points
Voltage Criteria (any of):

  1. R or S in limb leads ≥20 mm
  2. S in V1 or V2 ≥30 mm
  3. R in V5 or V6 ≥30 mm
ST-T Abnormalities:

  • ST-T vector opposite to QRS without digitalis
  • ST-T vector opposite to QRS with digitalis


Negative terminal P mode in V1 1 mm in depth and 0.04 sec in duration (indicates left atrial enlargement)
Left axis deviation (QRS of -30° or more) 2
QRS duration ≥0.09 sec 1
Delayed intrinsicoid deflection in V5 or V6 (>0.05 sec) 1

Other voltage-based criteria for LVH include:

  • Lead I: R wave > 14 mm
  • Lead aVR: S wave > 15 mm
  • Lead aVL: R wave > 12 mm
  • Lead aVF: R wave > 21 mm
  • Lead V5: R wave > 26 mm
  • Lead V6: R wave > 20 mm



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